Pharmacological Intervention to the Inflammatory Response from Decompression Sickness in Rats

Little, T; Butler, Bruce D

doi:10.3357/asem.2118.2008

Cited by 13 publications

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“…Decompression sickness (DCS) is the result of dissolved gas forming nitrogen bubbles in tissues and venous blood as an individual moves from a higher to a lower ambient pressure. Extravascular nitrogen bubbles can cause joint pain, localized infl ammation and edema [ 14 ] . Intravascular decompression may lead to venous and arterial gas embolization, pulmonary vascular obstruction, formation of edema, increased neutrophil activation and platelet aggregation [ 14 ] .…”

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Influence of Decompression Sickness on Vasomotion of Isolated Rat Vessels

et al. 2013

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Several studies have demonstrated that endothelial function is impaired following a dive even without decompression sickness. During this study we determined the effect of decompression sickness on endothelium-dependent and independent vasoreactivity. For this purpose twenty-seven male Sprague-Dawley rats were submitted to a simulated dive up to 1,000 kPa absolute pressure and divided into 3 groups: safe diving without decompression sickness or dives provoking mild or severe sickness. A fourth control group remained at atmospheric pressure. Endothelium-dependent and independent vasomotion was assessed ex vivo by measuring isometric tension in rings of abdominal aorta and mesenteric arteries. Dose-response curves were obtained with phenylephrine, acetylcholine and sodium nitroprusside. Acetylcholine-induced relaxation was measured in the presence of L-NAME, indometacin or both of them at once.Contraction was significantly decreased after each protocol compared with the control rats. Additionally, the response in animals from the severe group was significantly different from that of the safe and mild groups. Dose response curves for acetylcholine alone and in the presence of inhibitors remained unchanged. We did not observe differences in endothelium-dependent vasodilation after diving or in the presence of decompression sickness. Contractile response to phenylephrine was progressively impaired with increased decompression stress. These results may indicate smooth muscle injury.

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Influence of Decompression Sickness on Vasomotion of Isolated Rat Vessels

et al. 2013

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“…Several candidate agents, including dibutyryl cAMP (Little & Butler, 1997) and Zileuton, a leukotriene inhibitor (Little & Butler, 2008), have been investigated as a means of averting or moderating the inflammatory effects of C/D. Others, such as cortisol (Petrovsky et al, 1998) and melatonin (Carillo-Vico et al, 2005, 2006, also have been proposed as a means of alleviating the tissue-injury-induced inflammatory reactions.…”

Section: Discussionmentioning

confidence: 98%

“…Total protein from PLEU (mg/ml) and BAL (mg/g dry lung wt) fluids was assessed by a modified Lowry method, as previously described (Little & Butler, 2008), and adapted to a microplate reader at 750 nm (Pierce Chemical Company, Rockford, Illinois, USA). The analytical coefficient of variation (CV) for the intra-assay of protein in the normal range is 5.0-9.7%.…”

Section: Proteinmentioning

confidence: 99%

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Circadian Study of Decompression Sickness Symptoms and Response-Associated Variables in Rats

Butler¹,

Little²,

Sothern

et al. 2010

Chronobiology International

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In order to study circadian rhythms and decompression sickness (DCS), we determined: 1) the baseline circadian time structure in noncompressed rats of potential response variables to compression/decompression (C/D), and 2) whether rats subjected to C/D display a circadian time-dependent difference in inflammatory response intensity and biological tolerance. Subgroups of male rats, standardized to a 12 h light/12 h dark schedule, were evaluated every 4 h over 24 h after they were either compressed to 683 kPa (group E) or remained at sea level (group C). During 60 min recovery, evaluation included gross DCS symptoms and pulmonary edema in all E rats, and cell counts, nitric oxide, protein, thromboxane B(2,) and leukotriene E(4) levels in survivors. Chi-square, ANOVA, and 24 h cosinor analyses were used to test for time-of-day effects. C/D exposures near the end of dark/activity or during light/resting were generally better tolerated, with lowest signs of DCS symptoms and lowest responses by most of the variables monitored. More deaths were observed in the first half of the dark/activity span. Of the 16 subsets of inflammatory-associated variables, overall increases were observed in 13 and decreases in 2. Significant or borderline significant circadian time effects were found in 14 variables in group C, 12 variables in group E, and 13 variables in response (E%C). Thus, nearly all baseline indices of DCS demonstrated circadian time-dependencies in the sea-level exposed control rats (group C), and nearly all were modified by the circadian time of C/D. Such time-of-day effects of DCS are potentially relevant to the operational concerns of occupations involving decompression exposures and the investigation of prevention and treatment intervention strategies of DCS.

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“…Zafirlukast (ZA) ( Table 1) is a leukotriene antagonist marketed for the treatment of asthma, but has also recently been studied as mycobacterial growth inhibitor, and for treatment of decompression sickness (Little and Butler 2008;Pinault et al 2013). It is a poorly water soluble drug, that can best be described as a "brick dust" molecule (Timko et al, 1999).…”

Section: Introductionmentioning

confidence: 98%

Supersaturation of zafirlukast in fasted and fed state intestinal media with and without precipitation inhibitors

Madsen

Boyd

Rades

2016

European Journal of Pharmaceutical Sciences

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Pharmacological Intervention to the Inflammatory Response from Decompression Sickness in Rats

Abstract: The effect of inflammatory-like responses to DCS can be altered with pharmacological intervention given prior to compression.

Cited by 13 publications

References 0 publications

Influence of Decompression Sickness on Vasomotion of Isolated Rat Vessels

Influence of Decompression Sickness on Vasomotion of Isolated Rat Vessels

Circadian Study of Decompression Sickness Symptoms and Response-Associated Variables in Rats

Supersaturation of zafirlukast in fasted and fed state intestinal media with and without precipitation inhibitors

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